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Pulmonary Arterial Hypertension (PAH) is a severe progressive disease characterized by a sustained increase of pulmonary artery pressure resulting in heart failure and death (1). Current therapeutic approaches, including endothelin receptor antagonists such as macitentan, mainly provide symptomatic relief and some improvement of prognosis. Recent evidence has shown that Rho-associated coiledcoil forming protein kinases (ROCK), are relevant in the physiopathology of PAH due to their key roles on pulmonary arterial smooth muscle cell (SMC) contraction and proliferation. To validate the hypothesis that pharmacological ROCK inhibition may be beneficial in PAH we utilized a novel highly potent and selective ROCK inhibitor (2).